CV Flashcards
Cardiac tissue conduction velocity, arranged from fastest to slowest
Purkinje system > atrial muscle > ventricular muscle > AV node
“Park At Venture Avenue”
Adverse effects/contraindications of ACE inhibitors
Cough and angioedema d/t increased bradykinin
Contraindicated in C1 esterase deficiency (which causes hereditary angioedema: low C1 esterase leads to increased bradykinin activity)
Hyperkalemia, hypotension
Use w/ caution in bilateral renal artery stenosis (ACE I will further reduce GFR)
ACE I vs. ARB effect on angio I, angio II, renin, aldosterone, bradykinin
ACE I: increase renin, angio I and bradykinin / decrease angio II, aldosterone
ARB: increase renin, angio I, angio II / decrease aldosterone / no change to bradykinin
Beck’s triad for cardiac tamponade
Hypotension
Distended neck veins (JVD)
Muffled heart sounds
Will also have pulsus paradoxus (also seen with asthma/COPD, sleep apnea, pericarditis, croup)
Effect of hand grip maneuver on murmur intensity
increases afterload - increased intensity of MR, AR, VSD; decreased for HCM and AS. Later onset of MVP click/murmur
Effect of inspiration on heart sounds
increases venous return to RA; thus increases R heart sound intensity
Effect of valsalva on murmur intensity
decreases preload: decreases intensity of most murmurs (including AS), increases HCM. Earlier onset of MVP click/murmur
Effect of rapid standing on murmur intensity
(same as valsalva) - decreases preload: decreases intensity of most murmurs, except HCM (increased). Earlier onset of MVP click/murmur
Effect of rapid squatting on murmur intensity
increases venous return/preload/afterload
increases intensity of AS, MR, VSD; decreases HCM
later onset of MVP click/murmur
Equation for ejection fraction (EF)
EF = SV/EDV = (EDV-ESV)/EDV
EF is an index of ventricular contractility.
EF reduced in systolic HF (HFrEF), normal in diastolic HF (HFpEF)
Equation for factors contributing to BP
BP = CO * TPR
CO = HR * SV
SV depends on contractility and preload
Preload depends on venous tone & circulating blood volume (which is based on thirst, Na/H2O retention)
TPR depends on direct innervation (alpha receptors), circulating regulators (catetols, angio II), and local regulators (NO, prostacyclin, angio II, O2, H+, adenosine, endothelin)
Osler-Weber-Rendu syndrome
aka hereditary hemorrhagic telangiectasia. blanching lesions (telangiectasias) on skin/mucous membranes, recurrent epistaxis, skin discolorations, AVMs, GI bleeding, hematuria
Jervell and Lange-Nielsen syndrome vs. Romano-Ward syndrome
JVN: sensorineural deafness + congenital long QT (K+ channel) defect
RW: only congenital long QT (no deafness)
Pulmonary HTN drugs
Endothelin receptor blockers: reduce pulm vasc resistance. e.g. bosentan. Hepatotoxic (monitor LFTs)
PDE-5 inhibitors: prolonged vasodilation via NO
Prostacyclin analogs (PGI1): vasodilation of pulm and systemic arterial vasc beds; inhibition of platelet aggregation. e.g. epoprostenol, iloprost. Can cause flushing, jaw pain
Cardiac pressures in:
RA, RV, Pulm artery, LA, LV Aorta
RA: <5 (NICKEL) RV: 25/5 (QUARTER) Pulm artery: 25/10 (QUARTER) LA (approximated by PCWP): <10 (DIME) LV: 120/10 (DOLLAR) Aorta: 120/80 (systemic) (DOLLAR)
55 = 25, 1010 = 100 (to remember the order)
Equations for blood flow and resistance through a vessel
Q (flow) = (P1 -P2)*(r^4) / nL P1 - P2 = driving pressure (from high to low) r = radius of the vessel L = length of BV n = viscosity of blood
R (resistance) = nL/(r^4)
Presence of S3
Increased filling pressures e.g. with MR, HF. More common in dilated ventricles but can be normal (young kids, athletes, preg women). Best heard at apex in LLDP at end expiration
Presence of S4
Atrial kick; best heard at apex in LLDP at end expiration. Indicates high atrial P, assoc w/ ventricular noncompliance (e.g. HCM, LVH d/t AS or HTN). Always abnormal
CO equation using Fick’s principle
CO = (rate of O2 consumption)/(arteriovenous O2 difference)
a-v O2 diff calculated by arterial blood O2 content - venous content
Equation for blood O2 content
(O2 binding capacity)*(% saturation) + (dissolved O2)
Dissolved O2 = amount of o2 unbound to Hb (usually a small fraction of total blood O2 content)
Respiratory quotient
Ratio of CO2 to O2 across alveolar membrane. Used to estimate metabolic rate. Normal value ~ 0.8
Most common sites of atherosclerosis (from most to least common)
Abdominal aorta
Coronary artery
Popliteal artery
Carotid artery
“after I work out my ABs, I grab a CORONA and POP my collar up to my CAROTID”
Normal PO2 in R heart and L heart, and what changes in PO2 indicate
R heart: normally 40 mmHg; L heart: normally 104 mmHg. >40 in R circuit and <104 in L circuit suggests ASD (L –> R shunt). If the change in oxygenation is only seen in the ventricles and not the atria, suggests a VSD
Most specific finding for pulmonary arterial HTN
P2 louder than A2 (suggesting higher pressures in the pulmonary (R) circuit)
Baroreceptor activity with hypotension
Hypotension causes decreased stretch –> reduced baroreceptor firing, increased efferent SNS firing/decreased PSNS stim –> vasoconstriction; increased HR, contractility, BP
Baroreceptor activity with carotid massage
Carotid massage increases stretch, increasing baro firing, increased AV node refractory period and reduced HR
Cushing reflex
Triad of HTN, brady, resp depression:
Increased ICP constricts arterioles –> cerebral ischemia, increased pCO2 (CO2 vasodilates cerebral vasculature) / reduced pH –> central reflex SNS increase in PP (HTN) –> increased stretch –> peripheral baroreceptor-induced brady
Digoxin effects and toxicity, predisposing factors
- positive inotrope: indirectly increases intracellular Ca2+ by blocking the Na/K ATPase (this will increase Na+ in the cell, reducing the drive of the Na/Ca exchanger which normally brings in Na in xchng for Ca)
- negative chronotrope: stimulates vagus n. (PSNS), slowing conduction thru AV node (reduces HR)
- toxicity: blurry yellow vision, N/V, arrhythmias (d/t delayed after-depols caused by increased Ca), AV block, hyperkalemia. Tx w/ normalizing K+ slowly, cardiac pacer, anti-digoxin Fab, Mg2+
- risk factors: renal failure (can’t excrete), hypoK+ (permissive for digoxin binding site on Na/K ATPase), drugs that displace digoxin from tissue-binding sites, decreased clearance (verapamil, amiodarone, quinidine)
Causes of pulsus paradoxus
4 C’s:
- cardiac tamponade
- constrictive pericarditis
- COPD
- severe (“c-vere”) asthma
MI complications (and what cells are predominant at each stage)
- 1-3 days: PMN prominence; fibrinous pericarditis
- 2-7 days: macrophages; pap muscle rupture –> MR
- 3-5 days: macrophages; interventricular septal rupture –> VSD –> increased O2 sat and P in RV
- 5-14: macrophages; free wall rupture –> cardiac tamponade. LVH and previous MI protect against free wall rupture. Acutely, can lead to SCD
- 2 wks-months: collagen/scar; true ventricular aneurysm, assoc w/ fibrosis
- Several wks: collagen/scar; Dressler syndrome (late fibrinous pericarditis d/t AI phenomenon)
- LV failure and pulm edema: can be 2ndary to LV infarction, VSD, free wall rupture, pap muscle rupture w/ MR
Equation for flow rate through a blood vessel
Q = A*V where A = cross sectional area of vessel, and V = velocity of blood flow.
Remember that 1 cm^3 = 1 mL
A is relieved by sitting up and leaning forward; B is heard best with sitting up and leaning fwd
A: acute pericarditis
B: aortic regurgitation murmur
